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Renal ischemia-reperfusion (I/R) injury causes renal tubular necrosis, apoptosis, and inflammation leading to acute renal dysfunction. Recent studies have revealed that deletion of Gα12 mitigates the renal damage due to I/R injury. Our previous study showed that activation of dopamine D3 receptor (D3R) increased its linkage with Gα12, and hampered Gα12-mediated stimulation of renal sodium transport. In the present study, we used an in-vivo rat model and an in vitro study of the renal epithelial cell line (NRK52E) to investigate whether or not an increased linkage between D3R and Gα12 contributes to the protective effect of D3R on renal I/R injury.

Stimulation of Dopamine D3 Receptor Attenuates Renal Ischemia-Reperfusion Injury via Increased Linkage With Gα12